| First Author | Banerjee SK | Year | 2024 |
| Journal | Cell Rep | Volume | 43 |
| Issue | 7 | Pages | 114486 |
| PubMed ID | 38990718 | Mgi Jnum | J:391083 |
| Mgi Id | MGI:7708994 | Doi | 10.1016/j.celrep.2024.114486 |
| Citation | Banerjee SK, et al. (2024) Glucose transporter 1 is essential for the resolution of methicillin-resistant S. aureus skin and soft tissue infections. Cell Rep 43(7):114486 |
| abstractText | Skin/soft tissue infections (SSTIs) caused by methicillin-resistant Staphylococcus aureus (MRSA) pose a major healthcare burden. Distinct inflammatory and resolution phases comprise the host immune response to SSTIs. Resolution is a myeloid PPARgamma-dependent anti-inflammatory phase that is essential for the clearance of MRSA. However, the signals activating PPARgamma to induce resolution remain unknown. Here, we demonstrate that myeloid glucose transporter 1 (GLUT-1) is essential for the onset of resolution. MRSA-challenged macrophages are unsuccessful in generating an oxidative burst or immune radicals in the absence of GLUT-1 due to a reduction in the cellular NADPH pool. This translates in vivo as a significant reduction in lipid peroxidation products required for the activation of PPARgamma in MRSA-infected mice lacking myeloid GLUT-1. Chemical induction of PPARgamma during infection circumvents this GLUT-1 requirement and improves resolution. Thus, GLUT-1-dependent oxidative burst is essential for the activation of PPARgamma and subsequent resolution of SSTIs. |
